Humber Bridge: suppressing main cable corrosion by means of dehumidification

The Humber Bridge officially opened in 1981 and carries 4 lanes of traffic across the Humber Estuary between Barton and Hessle to the west of Kingston-upon-Hull in East Yorkshire, England. When opened, it was the longest span suspension bridge in the world with a main span of 1410m but it currently ranks as the fifth longest span in the world. Humber Bridge Board (HBB) commissioned an internal inspection of the main cables following the discovery of extensive corrosion and broken wires in the main cables of two older suspension bridges in the UK. The main cable inspections revealed widespread, if generally light corrosion with localised pitting and a very small number of broken wires. Dehumidification of suspension bridge main cables is becoming standard practice not only in the UK but worldwide. This paper examines the installation of the Humber Bridge system, discusses the mechanics of atmospheric steel corrosion and explains how the cable dehumidification system will suppress future corrosion

Additional file 2: Figure S2. of Epithelial requirement for in vitro proliferation and xenograft growth and metastasis of MDA-MB-468 human breast cancer cells: oncogenic rather than tumor-suppressive role of E-cadherin

a Comparison of individual tumor growth plots for 468-shCDH1-B and 468-shCDH1-D tumors to day of tumor harvest. b Tumor volumes at time mice were killed did not differ greatly. (PDF 106 kb

Fc Effector Function Contributes to the Activity of Human Anti-CTLA-4 Antibodies

(Summary) With the use of a mouse model expressing human Fc-gamma receptors (FcγRs), we demonstrated that antibodies with isotypes equivalent to ipilimumab and tremelimumab mediate intra-tumoral regulatory T (Treg) cell depletion in vivo, increasing the CD8+ to Treg cell ratio and promoting tumor rejection. Antibodies with improved FcγR binding profiles drove superior anti-tumor responses and survival. In patients with advanced melanoma, response to ipilimumab was associated with the CD16a-V158F high affinity polymorphism. Such activity only appeared relevant in the context of inflamed tumors, explaining the modest response rates observed in the clinical setting. Our data suggest that the activity of anti-CTLA-4 in inflamed tumors may be improved through enhancement of FcγR binding, whereas poorly infiltrated tumors will likely require combination approaches